A variety of theories have been proposed to explain sudden infant death syndrome (SIDS). SIDS is defined as "the sudden death of an infant or young child which is unexpectd by history, and in which a thorough post-mortem examination fails to reveal an adequate cause for death". While SIDS may occur for different reasons, one attribute of this phenomenon, included in the great majority of the cases described in the literature, is apnea (or respiratoray pause or periodic breathing) which occurs during sleep and is fatal. The autopsy reports describe conditions that are consistent with a condition of hypoxia and/or hypoxemia having existed for some time prior to the fatal apneic episode. It is the apneic character of SIDS which is addressed when "SIDS-risks" infants are placed on a cardiopulmonary monitor or treated with respiratory stimulants.
Some adult humans also suffer severe apnea during sleep (adult sleep apnea, or hypersomnia with periodic apnea [HPA]). SIDS and HPA share the fact that they occur during sleep, and that at least part of the apnea occurs without the subject's making any attempt to breathe. This latter condition is called "central apnea" because it appears to be ordered by the central nervous system. HPA oocurs most frequently in overweight males, over 40 years of age, who are given to strident or stentorian snoring. Typically, their obesity causes such individuals to sleep in a supine position. Careful observations have shown that they possess redundancy of tissue in the soft palate and the walls of the oropharynx. Part of this may be due to fatty deposit; part may be due to anatomical variation.
During sleep, especially "quiet sleep" or "REM (rapid eye-movement) sleep", facial muscles become hypotonic. During the inspiratory phase of the respiratory cycle the walls of the oropharynx and the base of the tongue tend to collapse onto the oropharynx. This is partly due to muscular hypotonia, partly due to negative pressure. The latter may be caused by negative intrathoracic pressure as air is breathed in, or by the Bernoulli effect (in which rapid airflow through a restricted space decreases the pressure).
It is the collapse of tissues into the oropharynx which produces central apnea. This occurs as the result of physical stimulation of the oropharyngeal wall, initiating a swallowing reflex during which respiration is suppressed. Occlusion of the oropharynx also causes an obstructive type of apnea, in which respiratory efforts are made against a blocked airway. Finally, mixed apneas occur in which an initial central phase is followed by an obstructive phase. Here the reflex cessation of breathing occurs, and when low oxygen and high carbon dioxide levels in the blood override the central apnea, the subject attempts to recommence breathing, but total obstruction has occured. If apneas are to be minimized in SIDS-risk infants or in adults with HPA, this encroachment on the oropharynx must be minimized.
When the head is flexed dorsally the cervical vertebrae and the cranial base are both moved away from the base of the tongue, whose upward and backward movement is prevented by its attchment through the strap muscles of the neck to the top of the sternum. Since the posterior pharyngeal wall is attched to the base of the cranium and the cervical vertebrae, dorsal head flexion increases space within the oropharynx. A device capable of maintaining slight dorsal flexion of the head during sleep, therefore, has the effect of ameliorating sleep apneas, whether in infants or adults.